Evidence for the role of lysosomes in the formation of prostaglandins during carrageenin induced inflammation in the rat

Anderson, Alan; Brocklehurst, W. E.; Willis, A.L.

doi:10.1016/s0031-6989(71)80006-1

Cited by 110 publications

(29 citation statements)

References 15 publications

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“…For example, in carrageenin-induced inflammation, although the onset of prostaglandin production apparently coincides with the migration of PMN leucocytes and mononuclear cells into the inflamed site (Anderson et al, 1971), elevated prostaglandin levels persist for longer than PMN leucocyte infiltration and remain elevated during the period of mononuclear cell predominance (Willis, 1969;DiRosa & Willoughby, 1971;DiRosa, Giroud & Willoughby, 1971). In contrast, in urate crystal-induced synovitis, the onset of prostaglandin production and several symptoms of inflammation precede PMN leucocyte accumulation (Glatt et al, 1974); moreover ingestion of urate crystals by synovial-lining macrophages also precedes the onset of vasodilatation, oedema and the subsequent 10 100 1000…”

Section: Discussionmentioning

confidence: 99%

“…However, the cellular origin of increased prostaglandin production in inflammatory reactions has remained uncertain and this aspect has received less attention than other criteria of mediator identification. The similar time course of appearance of prostaglandins, lysosomal enzymes and infiltrating leucocytes in carrageenin-induced exudates has been taken to suggest that the cellular infiltrate is the source of prostaglandin production (Anderson, Brocklehurst & Willis, 1971). The polymorphonuclear (PMN) leucocyte has been suggested as a possible source of inflammatory prostaglandins on the basis of observed in vitro prostaglandin E (PGE) production by rabbit PMN leucocytes (Higgs, McCall & Youlten, 1975).…”

Section: Introductionmentioning

confidence: 99%

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Prostaglandin Production by Macrophages and the Effect of Anti‐inflammatory Drugs

Bray¹,

Gordon

1978

British J Pharmacology

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Macrophages derived from peritoneal cavity inflammatory exudates of guinea‐pigs produced substantial amounts of prostaglandin E2‐like activity during in vitro culture, so providing the basis for an experimental model of prostaglandin production during inflammatory reactions. Dose‐related inhibition of prostaglandin biosynthesis was demonstrated by 16 acidic non‐steroidal anti‐inflammatory drugs. Seven anti‐inflammatory glucocorticosteroid preparations inhibited prostaglandin production in a dose‐related manner. The relative potencies of dexamethasone, prednisolone and hydrocortisone were consistent with clinical anti‐inflammatory ranking. Cortisone, however, failed to inhibit macrophage prostaglandin production. Three other agents used in the treatment of inflammatory joint diseases were examined. Sodium aurothiomalate inhibited prostaglandin production, although higher concentrations were toxic to macrophages. D‐Penicillamine did not affect macrophage prostaglandin production. Colchicine, in contrast, enhanced prostaglandin production at some concentrations. The probable significance of macrophages as a source of prostaglandins, during inflammatory responses, is discussed.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Prostaglandin Production by Macrophages and the Effect of Anti‐inflammatory Drugs

Bray¹,

Gordon

1978

British J Pharmacology

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“…40 In the present study, pretreatment with ELEVA at dose levels of 100, 200, 300 mg/ kg bw. decreased the levels of SGOT, SGPT, and ALP that were previously found to be increased in formalin induced experimental animals.…”

Section: Discussionmentioning

confidence: 76%

Anti-inflammatory screening of ethanolic leaf extract of Vernonia arborea Buch. –Ham.in formalin induced albino wistar rats

Sridharan¹,

Venkatramani²,

Janakiraman³

et al. 2016

IJPER

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Context:The therapeutic potential of the genus Vernonia has been well documented over the years. However the pharmacological potential of the plant Vernonia arborea (Asteraceae) has been relatively less explored. Objective: To investigate the antiinflammatory effect of the ethanol leaf extract of V. arborea against formalin induced inflammation in rats. Materials and methods: Formalin induced inflammation method was used to induce inflammation in rats.0.1 ml/kg body weight (b.w.) of formalin was administered to the rats via sub-plantar injection to induce inflammation. The rats were pretreated with ethanol leaf extract of V. arborea at concentrations of 100, 200 and 300 mg/kg b.w. once daily for 30 days. Indomethacin (25 mg/kg b.w.) was used as standard drug. Biochemical and hematological parameters along with levels of antioxidant enzymes were evaluated. Results: Administration of formalin reduced antioxidant enzyme levels, total RBC and Hb. Pretreatment with ethanol leaf extract of V.arborea at dose dependent levels significantly increased (p<0.05)the levels of the above parameters. A significant increase (p<0.05) in paw thickness, level of serum enzymes (Aspartate transaminase, Alanine transaminase, Alkaline phosphatase and Creatine kinase), Lipid peroxide and leucocytes was observed in the rats induced with formalin, while these levels were normalized on pretreatment with ethanol leaf extract of V.arborea. Conclusion: The results of the present investigation demonstrate the antioxidant and anti-inflammatory potential of the ethanol leaf extract of V.arborea. However, it is imperative to isolate and purify the active principles involved in the pharmacological potency of this plant and determine its mechanism of action.

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“…Accordingly, 0.2 ml of extract solution in ethanol (95%) at different concentrations (1,2,4,8,16,32 and 64 µg/ml, respectively) was added to 8 ml of 0.004% (w/v) stock solution of DPPH in ethanol (95%). The scavenging activity on the DPPH radical was determined by measuring the absorbance at 517 nm until the reaction reached the steady state, using a UV-visible spectrophotometer (Shimadzu, Tokyo, Japan).…”

Section: Dpph Radical Scavenging Assaymentioning

confidence: 99%

Molecular Mechanism of Formalin-Induced Toxicity and Its Management

Khatun¹,

Rana²,

Khan³

et al. 2015

AJLS

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Abstract:The use of formalin (40% formaldehyde) for the preservation of food in an illegal way becoming a serious health issue in developing countries including Bangladesh. We investigated the Formalin (FA)-induced organ toxicity in Swiss albino mice. FA induction caused the significant elevation of the liver enzyme, SGOT and SGPT; the MDA levels in the liver and brain. Among the fractions of methanol extract of L. globosus, ethyl acetate (EA) fraction significantly reduced the elevated biochemical parameters (FA vs FA + EA fraction, µKa/L); SGOT (78.4 ± 0.3 vs 14.3 ± 0.9), SGPT (100.5 ± 5.2 vs 14.6 ± 0.7), MDA in liver (10.9 ± 0.2 vs 5.6 ± 0.1) and MDA in brain (16.9 ± 0.2 vs 6.3 ± 0.2). Morphological analyses also supported the beneficial effect of EA fraction in FA-induced liver toxicity. FA induction caused the phosphorylation of JNK, member of mitogen activated protein kinase (MAPK) in both the liver and brain, which were completely abolished by the treatment of EA fraction of L. globosus. Chemical analyses showed that the EA fraction exhibited antioxidant and free radical scavenging properties. The protective effect of the EA fraction on the FA-induced toxicity by the modulation of oxidative inflammatory pathway by its antioxidant and free radical scavenging activity.

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Evidence for the role of lysosomes in the formation of prostaglandins during carrageenin induced inflammation in the rat

Cited by 110 publications

References 15 publications

Prostaglandin Production by Macrophages and the Effect of Anti‐inflammatory Drugs

Prostaglandin Production by Macrophages and the Effect of Anti‐inflammatory Drugs

Anti-inflammatory screening of ethanolic leaf extract of Vernonia arborea Buch. –Ham.in formalin induced albino wistar rats

Molecular Mechanism of Formalin-Induced Toxicity and Its Management

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